CARDIAC ARRHYTHMIAS IN NEONATE

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1 Introduction: CARDIAC ARRHYTHMIAS IN NEONATE DR. PANKAJ SAKHUJA Neonatologist Average heart rate in a healthy newborn is beats/min and the range is from beats/min. A normal (sinus) rhythm (fig 1) is characterized by normal upright P waves (lead I and avf), a normal PR interval ( msec) followed by a narrow QRS complex (< 80 msec). Arrhythmias are disorder of heart rate or rhythm that can range from benign to life threatening. This can result from abnormal impulse formation (automaticity), abnormal conduction (reentry, AV block), or both. Figure 1: Normal ECG Definitions: Increase automaticity -Autonomous repetitive depolarization of cardiac cells at a faster rate. Re-entry (fig 2) Electrical impulse recurrently travels in a tight circle within the atrium, AV node or ventricles. Figure 2: Re-entry Atrioventricular block (AV block) - Impairment of the conduction (delayed or absent) between the atria and ventricles. AV dissociation - Atria and ventricles beat independent of each other. Narrow QRS complex (<80 msec) - Rapid activation of the ventricles via the normal His-Purkinje system, suggests normal rhythm or that the arrhythmia originates above the ventricles.

2 Wide QRS (>80 msec) - Abnormally slow ventricular activation, suggests that the arrhythmia originates in the ventricles, or because of abnormalities within the His-Purkinje system (e.g. supraventricular tachycardia with aberrancy). Classification: Arrhythmia may be Supraventricular (Atrial, nodal) or ventricular in origin. They are classified based on their rate and rhythm. Arrhythmias Tachyarrhythmia Bradyarrhythmia Premature beats (Irregular rhythm) Supraventricular Ventricular Premature Premature (Narrow QRS) (Wide QRS) Atrial contractions Ventricular contractions (PAC) (PVC) Ventricular Tachycardia (VT) Ventricular fibrillation (VF) Sinus 1 st degree 2 nd degree Complete Bradycardia AV block AV block AV block Mobitz Type I Mobitz type II Reentry Automatic Focus Sino Atrial Intra-Atrial. Atrioventricular reentry (WPW and Concealed) Atrioventricular node reentry Atrial flutter Permanent form of junctional reciprocating tachycardia. Atrial fibrillation Sinus tachycardia Atrial ectopic tachycardia (AET), Junctional ectopic tachycardia

3 Incidence: Arrhythmias are found in 1-5% of newborns during first 10 days of life. The most common benign arrhythmia is Premature Atrial Beats that will disappear over the first month of life. The most common symptomatic arrhythmia in the neonatal period is SVT, which has an incidence of 1/ Complete heart block occurs in 1 in 15,000 to 1 in 20,000 live births. Clinical Features: The clinical presentation is variable and depends on the type, rate and the duration of the arrhythmia. During an arrhythmia, the heart may not be able to pump enough blood to the body. Lack of blood flow can damage the brain, heart, and other organs. Some neonates may remain asymptomatic while others may be seriously ill and develop signs of CCF and cardiogenic shock. They can tolerate rates of > 300 bpm and higher of SVT for hrs hours before signs of CCF develop. Tachyarrhythmia Sinus Tachycardia Etiology Fever, infection, hypovolemia, shock, dehydration, pain, anemia, medications, hyperthyroidism etc. ECG- Normal sinus rhythm with rate >180 bpm and < bpm. Figure 3: Sinus tachycardia Supraventricular (SVT) and Ventricular Tachycardia (VT) - SVT VT/VF Salient features Atrioventricular reentry (AVRT) Most Common (50% of all SVT.) Rapid sudden onset and termination. Responds well to management that block the AV node (vagal stimulation and Atrial Flutter (AF) Second most common (9-14% of all SVT) Does not respond to management that blocks the AV node. Treatment with adenosine is diagnostic - slows the heart rate and make flutter wave visible. Other Forms Very Rare. Very Rare. Presents with hemodynamic instability. Associated with severe medical illness (hypoxemia, shock, electrolyte imbalance catecholamine toxicity etc.) Can turn into ventricular fibrillation. Ventricular fibrillation is almost always agonal.

4 adenosine) ECG No beat-to-beat variation. (Regular RR interval) No clear discernible P waves Almost always narrow QRS complex. NB - Wide QRS beyond beats is extremely rare so the diagnosis of VT should be considered. Saw toothed flutter waves. Variable AV conduction from 1:1-4:1. Narrow QRS. Unique for each type. VT Retrograde or no visible P waves. AV dissociation. Wide QRS. VF Chaotic rhythm, coarse irregular pattern. No identifiable QRS complexes Figure 4:SVT Figure5: Atrial Flutter. Figure 6: VT Figure 7: VF Bradyarrhythmia Sinus Bradycardia Etiology Oversedation, medications (placental transfer), hypothermia, increase vagal tone (suctioning etc.), hypoxia, airleak, acidosis, CNS abnormalities, increased ICT, hypothyroidism, apnea of prematurity etc. ECG Normal rhythm with rates <80/100. Figure 8: Sinus bradycardia

5 AV Block Etiology Structural heart disease - Lesions associated with atrial dilatation (ASD, Epstein s TAPVD AVSD etc.) Disorder of AV node etc. Metabolic disorders Inflammatory disorders (myocarditis, endocarditis etc.) Medications (digoxin, beta blockers etc.) Figure 9: 1st Degree Block Figure 10:2 nd Degree AV block (type I) Figure 11:2 nd Degree Block (type 2) Figure 12: Complete Heart Block 1 ST Degree 2 ND Degree 3 RD Degree Mechanism Delayed AV conduction. Mobitz type 1 Salient features Never symptomatic Intermittent failure of AV conduction with prior PR prolongation. Seen in sleep or under anesthesia Reversed by catecholamine and vagolytic agents Mobitz type 2 Intermittent failure of AV conduction without prior PR prolongation. Frequently progresses to complete heart block. Not reversible with medications. Worse prognosis than type 1. (Complete Heart Block) Complete absence of AV conduction. Congenital May be associated with maternal SLE with anti Ro and anti La antibodies that disrupt formation of the normal conduction system. Prenatal symptom included hydrops fetalis. Acquired Rare. Mainly infective (viral myocarditis, HIV infection) or related to tumors Poor outlook without

6 intervention. ECG Prolongation of the PR interval. (>0.15 sec) Progressive prolongation of PR interval until after 3-4 cycles the P wave is not conducted. Fixed PR interval (normal or prolonged) Intermittent nonconduction of P wave at regular interval such as 2:1, 3:1. Variations of RR interval distinguish it from complete block. Atrial rate > ventricular rate. (P wave appear regularly at normal rate but not followed by QRS complex, which occurs at a much slower rate.) AV dissociation Regular R-R intervals and regular P- P intervals. Premature Beats Figure 11: Conducted PAC Figure 12:Blocked PAC Figure 13: PVC Mechanism PAC Focus in the atrium or proximal AV node that depolarizes before SA node. PVC Focus in the ventricle that depolarizes before the atrial beat is conducted. Salient features Very common. Can initiate or terminate SVT. ECG Three types of presentation 1. If ectopic depolarizes before the SA node - Premature P wave is conducted to the ventricles normally is followed by a normal and premature narrow QRS beat. 2. If ventricle is in its refractory period (blocked premature beat) - No QRS complex. 3. Intermediate between these two timings Less common than PACs Usually sporadic but sometimes occur after every other beat (bigeminy), every third beat (trigeminy) If occur in groups of two or more (ie couplets, triplets etc) are pathologic and may be marker of myocarditis or myocardial dysfunction Wide QRS without a preceding early P wave followed by a compensatory pause.

7 An aberrant and wide QRS. Investigations: Maternal history for any medical illness and medications.(lupus, beta blockers, antihypertensive etc.) Electrolyte, calcium magnesium levels. Blood gas for acidosis and hypoxia. ECG - 12 Lead. Holter - 24 hrs ECG monitoring. Echocardiogram to determine the ventricular function and possible presence of congenital heart disease. Chest radiograph Drug levels to evaluate toxicity Management: Principles Assess the hemodynamic status and obtain ECG simultaneously. Asymptomatic or mildly affected neonates o Pharmacological measures are tried first. Symptomatic Neonate o Immediate measures to resuscitate o Emergency treatment of the shock. o Cardioversion is required regardless of the mechanism of tachycardia. o Treat any aggravating and reversible factors, e.g. hypoglycemia, electrolyte imbalance, acidosis. Phases of management include o Acute therapy. o Chronic therapy. o Treatment of SVT Acute: Vagal stimulation o Transient blocks the AV conduction. o Use with IV line in place.

8 o Nasogatric stimulation or rectal stimulation o Bag filled with ice over the face and ears for 15 sec. o Don t perform carotid massage or apply orbital pressure o If tachycardia terminates and returns immediately, additional stimulation may not be effective. Adenosine o Transiently blocks AV node conduction o Diagnostic -Terminates or alter the AV relationship and assists with the diagnosis for most SVT. o Given by very rapid intravenous push. (Half-life is 10 sec or less). o Higher dose may be required in patients with low cardiac output. Antiarrhythmic Drugs o If vagal stimulation or adenosine fails to terminate an episode and the neonate is hemodynamically stable consider other drugs after the consultation with the pediatric cardiologist. o Usual first line drugs of choice - Digoxin and/or Beta-blockers. o Other Antiarrhythmic drugs - Amiodarone, Flecainide, Procainamide, Sotalol, Quinidine etc. o Verapamil is contraindicated in neonates. Cardioversion o Used only in symptomatic neonates. o Defibrillator must deliver very low amplitude shocks and have small paddles. o Narrow QRS- Synchronous mode. o Wide QRS - Synchronous mode initially but asynchronous mode might be needed. o Avoid skin burns o Neonates who have been treated with digoxin should receive a bolus of lidocaine (1mg/kg) before cardioversion to prevent ventricular arrhythmias. Pacing o Brief Atrial over drive at a rate higher than tachycardia might allow the termination of atrial tachycardias including atrial flutter. Chronic Wolff-Parkinson-White syndrome or if status is unknown: Propranolol, 0.5 mg/kg PO every 6 hrs. No documented accessory pathway: Digoxin, 5 micrograms/kg PO every 12 hr after initial loading. Transcatheter ablation of accessory pathway is reserved for life threatening medical refractory cases. Treatment of Ventricular Tachycardia Few or no symptoms Drugs like Propranolol, Mexiletine and Amiodarone are tried Symptomatic or seriously ill - Cardioversion Treatment of Bradyarrhythmia and Premature beats - (See flow charts)

9 Tachycardia Wide QRS (Mostly ventricular) Narrow QRS (SVT) Asymptomatic Symptomatic Attempt vagal maneuvers (Without delay in a symptomatic neonate) Lidocain Synchronous DC shock Symptomatic Asymptomatic Procainamide Asynchronous DC shock Establish vascular access quicker than obtaining defibrillator No yes Synchronous DC shock 0.5 j/kg Adenosine 50mcg/kg Synchronous DC shock 1 j/kg Adenosine 100mcg/kg Synchronous DC shock 2 j/kg Adenosine 250mcg/kg Discuss with the pediatric cardiologist for further management (For no response and/or chronic therapy) (Options include Digoxin, Propranolol, and Amiodarone etc. depending on the diagnosis)

10 Bradycardia Rarely requires treatment in otherwise normal babies with episodic rates of 70/min. Symptomatic Asymptomatic (treat only if very low ventricular rates (<50)) Manage Airway, Breathing and Circulation. Correct Metabolic derangements Treat the underline cause Atropine 0.02mg/kg (minimum dose -0.1mg/dose and max dose 2mg/dose) Isoprenaline 0.02micrograms/kg/min (max dose 0.5 micrograms /kg/min) TEMPORARY TRASVENOUS PACING Implantation of a permanent pacemaker might be necessary.

11 Premature beats/ Irregular Rhythm Resolves within few months Usually needs NO TREATMENT PAC PVC Do not treat with inotropes - worsens heart failure Needs treatment when Multiform (couplets/triplets) Short run of tachycardia Correct Hypoxia and Acidosis. Lidocaine or Amiodarone in case of emergency treatment. Consult Pediatric cardiologist for follow up and further management Further Reading: 1. Andrew D blaufox, Irregular heart rate in children: Up to date 2. Tricia Lacy Gomella.Arrhythmia. Neonatology: Management, Procedures, On-Call Problems, Diseases, and Drugs. Medicine, 6th Ed.Mc Graw Hill. 3. Stacy A.S Killen and Frank A. Fish. Fetal and Neonatal arrhythmias. Neoreviews.2008; 9: Anne M. Dublin.Arrhythmias in Newborn.Neoreviews.2000; 1;e Stephanie Burns Wechsler and Gill Wernovsky.Cardiac Disorders,Arrhythmias: Manual of Neonatal Care.7 th Edition: John P Cloherty, Lippincott Williams and Wilkins. 6. N.R.C Roberton. Arrhythmia. Textbook of Neonatology. 4thedition: N.R.C Roberton, Janet M. Rennie, Churchill Livingstone. 7. Mitchell I Cohen and Roy Jedeikin: Arrhythmias in the fetus and Newborn: Avery s Disease of the Newborn.8 th edition, Elsevier. 8. George F. Van Hare. Neonatal Arrhythmias:Disease of the fetus and Infant Fanaroff & Martin s Neonatal Perinatal medicine. 8 th edition, Vol 2,Mosby. 9. Neonatal Cardiac Arrhythmias. UCSF Children s Hospital at UCSF Medical Centre website.